It is amazing to me how people get into an uproar over the death of a lion and don’t do the same thing about people. Don’t get me wrong, I think hunting for sport is wrong. If you want to eat it then that’s fine. It is a waste of life to go out and shoot a beautiful, majestic animal, such as Cecil.
The words below are a repost from the Conservative Tribune.com and they do make sense so I want to share them with you. Have a blessed day. Shirley
Both social media and the progressive mainstream media have been in an uproar over the past few days about the death of “Cecil,” a 13-year-old lion in Zimbabwe.
Cecil was killed in an organized licensed hunt by a big game hunter, Minnesota dentist Dr. Walter Palmer, who has now gone into hiding after receiving numerous death threats from outraged animal rights activists.
However, it would appear that the outrage surrounding the death of Cecil is what is commonly known as a “First World Problem,” as residents of Zimbabwe were mostly unaware of, and really don’t care about, the death of just another lion.
“What lion?” was the response of acting Information Minister Prisca Mupfumira, after being asked about the death of Cecil.
Though the government had yet to give an official response to the lion hunt, local authorities opened an investigation into whether the professional guides who led the hunt abided by the rules and regulations in place for such things.
According to Yahoo News, that hasn’t stopped angry animal rights and anti-hunting activists from ruining the life of Dr. Palmer, with some calling for his arrest, extradition and even death for hunting the lion with a bow and arrow and finishing it off with a gun.
But most people in Zimbabwe don’t care about the dead lion, as they have much greater problems to deal with, such as an 80 percent unemployment rate, insane monetary inflation and a hugely corrupt government.
“Are you saying that all this noise is about a dead lion? Lions are killed all the time in this country,” said Tryphina Kaseke, a used-clothes hawker on the streets of Harare. “What is so special about this one?”
The truth is, most locals in Zimbabwe actually look forward to the big game hunts that Westerners engage in, as the high price tag for the hunts means money pumped into the local economy, not to mention the meat from such hunts is required by law to be given to local tribes and villages.
“Why are the Americans more concerned than us?” said Joseph Mabuwa, a 33-year-old father of two. “We never hear them speak out when villagers are killed by lions and elephants in Hwange.”
Lions and other large animals are typically viewed as dangerous by the local population, and if these animals are not hunted, their populations will explode and bring about all sorts of other issues, like rampant disease and increased attacks on people.
If only as much outrage over a dead and dismembered lion were directed at those who kill and dismember hundreds of thousands of babies per year, our society might have a moral leg to stand on.
This article came out from ABC News and it got me to thinking about if I am afraid of catching the disease but I am afraid for my children and Grandchildren. I don’t think I’m afraid but I do have a chance of being exposed through my husband who flies out of Washington DC frequently. Thousands of people fly out of the airport he uses daily. He returned from a trip a week ago. What if that first case was on his plane flying into Dallas? It gives one a lot to think about.
Are you afraid of being exposed? For me personally I have to leave it in God’s hands and stay vigilant. The article below gives you some info that you need to know.
The deadly Ebola virus has arrived in the United States with the first diagnosis on American soil this week, bringing national attention back to the outbreak that has ravaged West Africa.
Health officials confirmed that a patient in Dallas was diagnosed with Ebola about a week after arriving from Liberia to visit family on Sept. 20. The patient was placed in isolation Sept. 28, but may have exposed five school age children in the days between arriving in Texas and being isolated.
“There is no doubt in my mind we will stop it here,” Centers for Disease Control and Prevention Director Dr. Thomas Frieden said at a news conference.
Ebola has killed 3,338 people and infected 3,840 others since the outbreak began in March, making it the worst outbreak since the virus was discovered in 1976. More people have died from Ebola in the last seven months than in every other Ebola outbreak to date combined, according to data from the World Health Organization.
Although those who have received care on American soil have generally fared well, WHO officials have said that the world needs to do more to stop the outbreak in Africa and keep it from expanding.
The CDC warned that the outbreak could reach 1.4 million cases by the end of January without proper intervention. But with additional resources and intervention, the outbreak could be over by about the same time, the agency said.
Here’s what you need to know about the Ebola virus
What Is Ebola?
The Ebola virus is as a group of viruses that cause a deadly kind of hemorrhagic fever. The term “hemorrhagic fever” means it causes bleeding inside and outside the body. The virus has a long incubation period of approximately eight to 21 days. Early symptoms include fever, muscle weakness, sore throat and headaches.
As the disease progresses, the virus can impair kidney and liver function and lead to external and internal bleeding. It’s one of the most deadly viruses on Earth with a fatality rate that can reach between approximately 50 to 90 percent. There is no cure.
How Is It Transmitted?
The virus is transmitted through contact with blood or secretions from an infected person, either directly or through contaminated surfaces, needles or medical equipment. A patient is not contagious until he or she starts showing signs of the disease.
Thankfully, the virus is not airborne, which means a person cannot get the disease simply by breathing the same air as an infected patient.
Where Did the Virus Come From?
The dangerous virus gets its name from the Ebola River in the Democratic Republic of Congo, which was near the site of one of the first outbreaks. The virus was first reported in 1976 in two almost simultaneous outbreaks in the Sudan and the Democratic Republic of Congo. They killed 151 and 280 people, respectively.
Certain bats living in tropical African forests are thought to be the natural hosts of the disease. The initial transmission of an outbreak usually results from a wild animal infecting a human, according to the WHO. Once the disease infects a person, it is easily transmissible between people in close contact.
Until this outbreak, approximately 2,361 people had been infected since the disease was identified in 1976. More than 1,548 of those infected died from it.
How Is It Transmitted?
The virus is transmitted through contact with blood or secretions from an infected person, either directly or through contaminated surfaces, needles or medical equipment. A patient is not contagious until he or she starts showing signs of the disease.
Thankfully, the virus is not airborne, which means a person cannot get the disease simply by breathing the same air as an infected patient.
Who Is At Risk?
The virus is not airborne, which means those in close contact can be infected and are most at risk. A person sitting next to an infected person, even if they are contagious, is not extremely likely to be infected.
Health workers and caregivers of the sick are particularly at risk for the disease because they work in close contact with infected patients during the final stages of the disease when the virus can cause internal and external bleeding.
In this outbreak alone, more than 100 health workers have been infected and at least 50 of them have died, according to the WHO.
The weather here in Oklahoma has been over 100 for the past several days. I have stayed close to the air-conditioning to stay comfortable. I was remembering this morning when I was a kid, it was nothing to have summers with temps at 110 that lasted for many days. We didn’t have air conditioning but we always had a good trusty box fan to blow hot air around. That was a big help. Anything to keep the air moving because with the humidity if it wasn’t moving it felt as if it were taking your breath away.
At this point you’re probably wondering why I titled this blog Life in Texas in 1850. That has to do with a branch of my family that lived on the Red River during that time. I can’t even begin to understand what their life was really like. I know it was at times almost intolerable and at other times laughter was happening because that is life.
A family had to worry about survival on a more intimate basis than we are. You know, just even getting hot water was a chore, not only in hauling, but then you had to heat it up. So, all the daily chores than required a lot more forethought—as well as just physical labor. Men, women and children—everybody’s working towards family survival. It didn’t matter if it was 110 outside that fire still had to be built. It went on every day of their life. The struggle to survive.
We take so much for granted in this day and time. How do you think you would do without electricity and running water? The family back then did what they had to do. That was the life they knew and was accustomed to living. I have a great appreciation and respect for what people have accomplished in the past. Imagine what our life would be like today if our families had not dealt with the life they had.
Have a blessed day.
Hello because of the research I did on Yellow fever epidemics for my book “Dobyns Chronicles.” Buy Here: http://www.amazon.com/dp/BOOKNMM468 I thought I would share it with you.
Yellow fever epidemics struck the United States repeatedly in the 18th and 19th centuries. The disease was not indigenous; epidemics were imported by ship from the Caribbean. Prior to 1822, yellow fever attacked cities as far north as Boston, but after 1822 it was restricted to the south. Port cities were the primary targets, but the disease occasionally spread up the Mississippi River system in the 1800s. New Orleans, Mobile, Savannah, and Charleston were major targets; Memphis suffered terribly in 1878. Yellow fever epidemics caused terror, economic disruption, and some 100,000-150,000 deaths. Recent white immigrants to southern port cities were the most vulnerable; local whites and blacks enjoyed considerable resistance. As you read it killed thousands so we have been blessed as a country to not have it now. It had to be scarey times back then. Did you have relatives who died from Yellow Fever.
This information is from Wikipedia
Yellow fever, known historically as yellow jack or yellow plague is an acute viral disease. In most cases symptoms include fever, chills, loss of appetite, nausea, muscle pains particularly in the back, and headaches. Symptoms typically improve within five days. In some people within a day of improving the fever comes back, there is abdominal pain, and liver damage begins causing yellow skin. If this occurs there is also an increased risk of bleeding and kidney problems.
The disease is caused by the yellow fever virus and is spread by the bite of the female mosquito. It only infects humans, other primates and several species of mosquito. In cities it is primarily spread by mosquitoes of the Aedes aegypti species. The virus is an RNA virus of the genus Flavivirus. The disease may be difficult to tell apart from other illnesses, especially in the early stages. To confirm a suspected case blood sample testing with PCR is required.
A safe and effective vaccine against yellow fever exists and some countries require vaccinations for travelers. Other efforts to prevent infection include reducing the population of the transmitting mosquito. In areas where yellow fever is common and vaccination is uncommon, early diagnosis of cases and immunization of large parts of the population is important to prevent outbreaks. Once infected, management is symptomatic with no specific measures effective against the virus. In those with severe disease death occurs in about half of people without treatment.
Yellow fever causes 200,000 infections and 30,000 deaths every year, with nearly 90% of these occurring in Africa. Nearly a billion people live in an area of the world where the disease is common. It is common in tropical areas of South America and Africa, but not in Asia. Since the 1980s, the number of cases of yellow fever has been increasing. This is believed to be due to fewer people being immune, more people living in cities, people moving frequently, and changing climate. The disease originated in Africa, where it spread to South America through the slave trade in the 17th century. Since the 17th century, several major outbreaks of the disease have occurred in the Americas, Africa, and Europe. In the 18th and 19th century, yellow fever was seen as one of the most dangerous infectious diseases. The yellow fever virus was the first human virus discovered.
Signs and symptoms
Yellow fever begins after an incubation period of three to six days. Most cases only cause a mild, infection with fever, headache, chills, back pain, loss of appetite, nausea, and vomiting. In these cases the infection lasts only three to four days.
In fifteen percent of cases, however, sufferers enter a second, toxic phase of the disease with recurring fever, this time accompanied by jaundice due to liver damage, as well as abdominal pain. Bleeding in the mouth, the eyes, and the gastrointestinal tract will cause vomit containing blood, hence the Spanish name for yellow fever, vomito negro (“black vomit”). The toxic phase is fatal in approximately 20% of cases, making the overall fatality rate for the disease 3% (15% * 20%). In severe epidemics, the mortality may exceed 50%.
Surviving the infection provides lifelong immunity, and normally there is no permanent organ damage.
Yellow fever virus
Group: Group IV ((+)ssRNA)
Species: Yellow fever virus
Yellow fever is caused by the yellow fever virus, a 40 to 50 nm wide enveloped RNA virus, the type species and namesake of the family Flaviviridae. It was the first illness shown to be transmissible via filtered human serum and transmitted by mosquitoes, by Walter Reed around 1900. The positive sense single-stranded RNA is approximately 11,000 nucleotides long and has a single open reading frame encoding a polyprotein. Host proteases cut this polyprotein into three structural (C, prM, E) and seven non-structural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B, NS5); the enumeration corresponds to the arrangement of the protein coding genes in the genome. Yellow fever belongs to the group of hemorrhagic fevers.
The viruses infect, amongst others, monocytes, macrophages and dendritic cells. They attach to the cell surface via specific receptors and are taken up by an endosomal vesicle. Inside the endosome, the decreased pH induces the fusion of the endosomal membrane with the virus envelope. The capsid enters the cytosol, decays, and releases the genome. Receptor binding as well as membrane fusion are catalyzed by the protein E, which changes its conformation at low pH, causing a rearrangement of the 90 homodimers to 60 homotrimers.
After entering the host cell, the viral genome is replicated in the rough endoplasmic reticulum (ER) and in the so-called vesicle packets. At first, an immature form of the virus particle is produced inside the ER, whose M-protein is not yet cleaved to its mature form and is therefore denoted as prM (precursor M) and forms a complex with protein E. The immature particles are processed in the Golgi apparatus by the host protein furin, which cleaves prM to M. This releases E from the complex which can now take its place in the mature, infectious virion.
Aedes aegypti feeding
Adults of the yellow fever mosquito Aedes aegypti. The male is on the left, females are on the right. Only the female mosquito bites can transmit the disease.
Yellow fever virus is mainly transmitted through the bite of the yellow fever mosquito Aedes aegypti, but other mosquitoes such as the tiger mosquito (Aedes albopictus) can also serve as a vector for this virus. Like other Arboviruses which are transmitted via mosquitoes, the yellow fever virus is taken up by a female mosquito when it ingests the blood of an infected human or other primate. Viruses reach the stomach of the mosquito, and if the virus concentration is high enough, the virions can infect epithelial cells and replicate there. From there they reach the haemocoel (the blood system of mosquitoes) and from there the salivary glands. When the mosquito next sucks blood, it injects its saliva into the wound, and the virus reaches the bloodstream of the bitten person. There are also indications for transovarial and transstadial transmission of the yellow fever virus within A. aegypti, that is, the transmission from a female mosquito to her eggs and then larvae. This infection of vectors without a previous blood meal seems to play a role in single, sudden breakouts of the disease.
There are three epidemiologically different infectious cycles, in which the virus is transmitted from mosquitoes to humans or other primates. In the “urban cycle,” only the yellow fever mosquito Aedes aegypti is involved. It is well adapted to urban centres and can also transmit other diseases, including dengue fever and chikungunya. The urban cycle is responsible for the major outbreaks of yellow fever that occur in Africa. Except in an outbreak in 1999 in Bolivia, this urban cycle no longer exists in South America.
Besides the urban cycle there is, both in Africa and South America, a sylvatic cycle (forest cycle or jungle cycle), where Aedes africanus (in Africa) or mosquitoes of the genus Haemagogus and Sabethes (in South America) serve as vectors. In the jungle, the mosquitoes infect mainly non-human primates; the disease is mostly asymptomatic in African primates. In South America, the sylvatic cycle is currently the only way humans can infect each other, which explains the low incidence of yellow fever cases on the continent. People who become infected in the jungle can carry the virus to urban centres, where Aedes aegypti acts as a vector. It is because of this sylvatic cycle that yellow fever cannot be eradicated.
In Africa there is a third infectious cycle, also known as “savannah cycle” or intermediate cycle, which occurs between the jungle and urban cycle. Different mosquitoes of the genus Aedes are involved. In recent years, this has been the most common form of transmission of yellow fever in Africa.
After transmission of the virus from a mosquito, the viruses replicate in the lymph nodes and infect dendritic cells in particular. From there they reach the liver and infect hepatocytes (probably indirectly via Kupffer cells), which leads to eosinophilic degradation of these cells and to the release of cytokines. Necrotic masses known as Councilman bodies appear in the cytoplasm of hepatocytes.
Fatality may occur when cytokine storm, shock, and multiple organ failure follow.
Yellow fever is a clinical diagnosis, which often relies on the whereabouts of the diseased person during the incubation time. Mild courses of the disease can only be confirmed virologically. Since mild courses of yellow fever can also contribute significantly to regional outbreaks, every suspected case of yellow fever (involving symptoms of fever, pain, nausea and vomiting six to ten days after leaving the affected area) is treated seriously.
If yellow fever is suspected, the virus cannot be confirmed until six to ten days after the illness. A direct confirmation can be obtained by reverse transcription polymerase chain reaction where the genome of the virus is amplified. Another direct approach is the isolation of the virus and its growth in cell culture using blood plasma; this can take one to four weeks.
Serologically, an enzyme linked immunosorbent assay during the acute phase of the disease using specific IgM against yellow fever or an increase in specific IgG-titer (compared to an earlier sample) can confirm yellow fever. Together with clinical symptoms, the detection of IgM or a fourfold increase in IgG-titer is considered sufficient indication for yellow fever. Since these tests can cross-react with other flaviviruses, like Dengue virus, these indirect methods cannot conclusively prove yellow fever infection.
Liver biopsy can verify inflammation and necrosis of hepatocytes and detect viral antigens. Because of the bleeding tendency of yellow fever patients, a biopsy is only advisable post mortem to confirm the cause of death.
In a differential diagnosis, infections with yellow fever have to be distinguished from other feverish illnesses like malaria. Other viral hemorrhagic fevers, such as Ebola virus, Lassa virus, Marburg virus and Junin virus, have to be excluded as cause.
Personal prevention of yellow fever includes vaccination as well as avoidance of mosquito bites in areas where yellow fever is endemic. Institutional measures for prevention of yellow fever include vaccination programs and measures of controlling mosquitoes. Programs for distribution of mosquito nets for use in homes are providing reductions in cases of both malaria and yellow fever.
The cover of a certificate that confirms that the holder has been vaccinated against yellow fever
Main article: Yellow fever vaccine
Vaccination is recommended for those traveling to affected areas, because non-native people tend to suffer more severe illness when infected. Protection begins by the tenth day after vaccine administration in 95% of people, and lasts for at least 10 years. About 81% of people are still immune after 30 years. The attenuated live vaccine stem 17D was developed in 1937 by Max Theiler. The WHO recommends routine vaccinations for people living in affected areas between the 9th and 12th month after birth. Up to one in four people experience fever, aches, and local soreness and redness at the site of injection.
In rare cases (less than one in 200,000 to 300,000), the vaccination can cause yellow fever vaccine-associated viscerotropic disease (YEL-AVD), which is fatal in 60% of cases. It is probably due to the genetic morphology of the immune system. Another possible side effect is an infection of the nervous system, which occurs in one in 200,000 to 300,000 cases, causing yellow fever vaccine-associated neurotropic disease (YEL-AND), which can lead to meningoencephalitis and is fatal in less than 5% of cases.
In 2009, the largest mass vaccination against yellow fever began in West Africa, specifically Benin, Liberia, and Sierra Leone. When it is completed in 2015, more than 12 million people will have been vaccinated against the disease. According to the World Health Organization (WHO), the mass vaccination cannot eliminate yellow fever because of the vast number of infected mosquitoes in urban areas of the target countries, but it will significantly reduce the number of people infected. The WHO plans to continue the vaccination campaign in another five African countries—Central African Republic, Ghana, Guinea, Côte d’Ivoire, and Nigeria—and stated that approximately 160 million people in the continent could be at risk unless the organization acquires additional funding to support widespread vaccinations.
In 2013, the World Health Organization stated “a single dose of vaccination is sufficient to confer life-long immunity against yellow fever disease.”
Some countries in Asia are theoretically in danger of yellow fever epidemics (mosquitoes with the capability to transmit yellow fever and susceptible monkeys are present), although the disease does not yet occur there. To prevent introduction of the virus, some countries demand previous vaccination of foreign visitors if they have passed through yellow fever areas. Vaccination has to be proven in a vaccination certificate which is valid 10 days after the vaccination and lasts for 10 years. A list of the countries that require yellow fever vaccination is published by the WHO. If the vaccination cannot be conducted for some reasons, dispensation may be possible. In this case, an exemption certificate issued by a WHO approved vaccination center is required.
Although 32 of 44 countries where yellow fever occurs endemically do have vaccination programmes, in many of these countries, less than 50% of their population is vaccinated.
Information campaign for prevention of dengue and yellow fever in Paraguay
Control of the yellow fever mosquito Aedes aegypti is of major importance, especially because the same mosquito can also transmit dengue fever and chikungunya disease. A. aegypti breeds preferentially in water, for example in installations by inhabitants of areas with precarious drinking water supply, or in domestic waste; especially tires, cans and plastic bottles. These conditions are common in urban areas in developing countries.
Two main strategies are employed to reduce mosquito populations. One approach is to kill the developing larvae. Measures are taken to reduce the water accumulations in which the larva develops. Larvicides are used, as well as larva-eating fish and copepods, which reduce the number of larvae. For many years, copepods of the genus Mesocyclops have been used in Vietnam for preventing dengue fever. It eradicated the mosquito vector in several areas. Similar efforts may be effective against yellow fever. Pyriproxyfen is recommended as a chemical larvicide, mainly because it is safe for humans and effective even in small doses.
The second strategy is to reduce populations of the adult yellow fever mosquito. Lethal ovitraps can reduce Aedes populations, but with a decreased amount of pesticide because it targets the mosquitoes directly. Curtains and lids of water tanks can be sprayed with insecticides, but application inside houses is not recommended by the WHO. Insecticide-treated mosquito nets are effective, just as they are against the Anopheles mosquito that carries malaria.
As for other flavivirus infections, there is no cure for yellow fever. Hospitalization is advisable and intensive care may be necessary because of rapid deterioration in some cases. Different methods for acute treatment of the disease have been shown to not be very successful; passive immunisation after emergence of symptoms is probably without effect. Ribavirin and other antiviral drugs as well as treatment with interferons do not have a positive effect in patients. A symptomatic treatment includes rehydration and pain relief with drugs like paracetamol (known as acetaminophen in the United States). Acetylsalicylic acid (aspirin) should not be given because of its anticoagulant effect, which can be devastating in the case of internal bleeding that can occur with yellow fever.
Endemic range of yellow fever in South America (2009)
Endemic range of yellow fever in Africa (2009)
Yellow fever is endemic in tropical and subtropical areas of South America and Africa. Even though the main vector (Aedes aegypti) also occurs in tropical and subtropical regions of Asia, the Pacific and Australia, yellow fever does not occur in these parts of the globe. Proposed explanations include the idea that the strains of the mosquito in the East are less able to transmit the yellow fever virus, that immunity is present in the populations because of other diseases caused by related viruses (for example, dengue), and that the disease was never introduced because the shipping trade was insufficient, but none are considered satisfactory.   Another recent proposal is the absence of a slave trade to Asia on the scale of that to the Americas.  The trans-Atlantic slave trade was probably the means of introduction into the Western hemisphere from Africa.  Worldwide there are about 600 million people living in endemic areas. WHO officially estimates that there are 200,000 cases of disease and 30,000 deaths a year; the number of officially reported cases is far lower. An estimated 90% of the infections occur on the African continent. In 2008, the largest number of recorded cases were in Togo.
Phylogenetic analysis identified seven genotypes of yellow fever viruses, and it is assumed that they are differently adapted to humans and to the vector Aedes aegypti. Five genotypes (Angola, Central/East Africa, East Africa, West Africa I, and West Africa II) occur only in Africa. West Africa genotype I is found in Nigeria and the surrounding areas. This appears to be especially virulent or infectious as this type is often associated with major outbreaks. The three genotypes in East and Central Africa occur in areas where outbreaks are rare. Two recent outbreaks in Kenya (1992–1993) and Sudan (2003 and 2005) involved the East African genotype, which had remained unknown until these outbreaks occurred.
In South America, two genotypes have been identified (South American genotype I and II). Based on phylogenetic analysis these two genotypes appear to have originated in West Africa and were first introduced into Brazil. The date of introduction into South America appears to be 1822 (95% confidence interval 1701 to 1911). The historical record shows that there was an outbreak of yellow fever in Recife, Brazil, between 1685 and 1690. The disease seems to have disappeared, with the next outbreak occurring in 1849. It seems likely that it was introduced with the importation of slaves through the slave trade from Africa. Genotype I has been divided into five subclades, A through E.
The evolutionary origins of yellow fever most likely lie in Africa, with transmission of the disease from primates to human beings. It is thought that the virus originated in East or Central Africa and spread from there to West Africa. As it was endemic in Africa, the natives had developed some immunity to it. When an outbreak of yellow fever would occur in an African village where colonists resided, most Europeans died, while the native population usually suffered nonlethal symptoms resembling influenza. This phenomenon, in which certain populations develop immunity to yellow fever due to prolonged exposure in their childhood, is known as acquired immunity. The virus, as well as the vector A. aegypti, were probably transferred to North and South America with the importation of slaves from Africa, part of the Columbian Exchange following European exploration and colonization.
The first definitive outbreak of yellow fever in the New World was in 1647 on the island of Barbados. An outbreak was recorded by Spanish colonists in 1648 in Yucatán, Mexico, where the indigenous Mayan people called the illness xekik (“blood vomit”). In 1685, Brazil suffered its first epidemic, in Recife. The first mention of the disease by the name “yellow fever” occurred in 1744.
Although yellow fever is most prevalent in tropical-like climates, the Northern United States was not exempted from the fever. The first outbreak in English-speaking North America occurred in New York in 1668, and a serious one afflicted Philadelphia in 1793. English colonists in Philadelphia and the French in the Mississippi River Valley recorded major outbreaks in 1669, as well as those occurring later in the eighteenth and nineteenth centuries. The southern city of New Orleans was plagued with major epidemics during the nineteenth century, most notably in 1833 and 1853. At least 25 major outbreaks took place in the Americas during the eighteenth and nineteenth centuries, including particularly serious ones in Cartagena in 1741, Cuba in 1762 and 1900, Santo Domingo in 1803, and Memphis in 1878. Major outbreaks have also occurred in southern Europe. Gibraltar lost many to an outbreak in 1804, in 1814, and again in 1828. Barcelona suffered the loss of several thousand citizens during an outbreak in 1821. Urban epidemics continued in the United States until 1905, with the last outbreak affecting New Orleans.
Due to yellow fever, in Colonial times and during the Napoleonic Wars the West Indies were known as a particularly dangerous posting for soldiers. Both English and French forces posted there were decimated by the “Yellow Jack.” Wanting to regain control of the lucrative sugar trade in Saint-Domingue, and with an eye on regaining France’s New World empire, Napoleon sent an army under the command of his brother-in-law to Saint-Domingue to seize control after a slave revolt. The historian J. R. McNeill asserts that yellow fever accounted for approximately 35,000 to 45,000 casualties of these forces during the fighting. Only one-third of the French troops survived for withdrawal and return to France. Napoleon gave up on the island, and in 1804 Haiti proclaimed its independence as the second republic in the western hemisphere.
Yellow Fever Epidemic of 1878 can still be found in New Orleans’ cemeteries.
The yellow fever epidemic of 1793 in Philadelphia, which was then the capital of the United States, resulted in the deaths of several thousand people, more than nine percent of the population. The national government fled the city, including President George Washington. Additional yellow fever epidemics struck Philadelphia, Baltimore and New York in the eighteenth and nineteenth centuries, and traveled along steamboat routes from New Orleans. They caused some 100,000–150,000 deaths in total.
In 1858 St. Matthew’s German Evangelical Lutheran Church in Charleston, South Carolina, suffered 308 yellow fever deaths, reducing the congregation by half. In 1873, Shreveport, Louisiana lost almost a quarter of its population to yellow fever. In 1878, about 20,000 people died in a widespread epidemic in the Mississippi River Valley. That year, Memphis had an unusually large amount of rain, which led to an increase in the mosquito population. The result was a huge epidemic of yellow fever. The steamship John D. Porter took people fleeing Memphis northward in hopes of escaping the disease, but passengers were not allowed to disembark due to concerns of spreading yellow fever. The ship roamed the Mississippi River for the next two months before unloading her passengers. The last major U.S. outbreak was in 1905 in New Orleans.
Ezekiel Stone Wiggins, known as the Ottawa Prophet, proposed that the cause of a Yellow fever epidemic in Jacksonville, Florida, in 1888 was astronomical.
The planets were in the same line as the sun and earth and this produced, besides Cyclones, Earthquakes, etc., a denser atmosphere holding more carbon and creating microbes. Mars had an uncommonly dense atmosphere, but its inhabitants were probably protected from the fever by their newly discovered canals, which were perhaps made to absorb carbon and prevent the disease.
Yellow fever in Buenos Aires, 1871
Carlos Finlay, a Cuban doctor and scientist, first proposed in 1881 that yellow fever might be transmitted by mosquitoes rather than direct human contact. Since the losses from yellow fever in the Spanish–American War in the 1890s were extremely high, Army doctors began research experiments with a team led by Walter Reed, composed of doctors James Carroll, Aristides Agramonte and Jesse William Lazear. They successfully proved Finlay’s ″Mosquito Hypothesis.″ Yellow fever was the first virus shown to be transmitted by mosquitoes. The physician William Gorgas applied these insights and eradicated yellow fever from Havana. He also campaigned against yellow fever during the construction of the Panama Canal, after a previous effort on the part of the French failed (in part due to mortality from the high incidence of yellow fever and malaria, which decimated the workers).
Although Dr. Reed has received much of the credit in United States history books for “beating” yellow fever, he had fully credited Dr. Finlay with the discovery of the yellow fever vector, and how it might be controlled. Dr. Reed often cited Finlay’s papers in his own articles, and also gave him credit for the discovery in his personal correspondence. The acceptance of Finlay’s work was one of the most important and far-reaching effects of the Walter Reed Commission of 1900. Applying methods first suggested by Finlay, the United States government and Army eradicated yellow fever in Cuba and later in Panama, allowing completion of the Panama Canal. While Dr. Reed built on the research of Carlos Finlay, historian François Delaporte notes that yellow fever research was a contentious issue. Scientists, including Finlay and Reed, became successful by building on the work of less prominent scientists, without always giving them the credit they were due. Dr. Reed’s research was essential in the fight against yellow fever. He should also receive full credit for his use of the first type of medical consent form during his experiments in Cuba, an attempt to ensure that participants knew they were taking a risk by being part of testing.
During 1920–1923, the Rockefeller Foundation’s International Health Board (IHB) undertook an expensive and successful yellow fever eradication campaign in Mexico. The IHB gained the respect of Mexico’s federal government because of the success. The eradication of yellow fever strengthened the relationship between the US and Mexico, which had not been very good in the past. The eradication of yellow fever was also a major step toward better global health.
In 1927, scientists isolated the yellow fever virus in West Africa. Following this, two vaccines were developed in the 1930s. The vaccine 17D was developed by the South African microbiologist Max Theiler at the Rockefeller Institute in New York City. This vaccine was widely used by the U.S. Army during World War II. Following the work of Ernest Goodpasture, Theiler used chicken eggs to culture the virus and won a Nobel Prize in 1951 for this achievement. A French team developed the French neurotropic vaccine (FNV), which was extracted from mouse brain tissue. Since this vaccine was associated with a higher incidence of encephalitis, FNV was not recommended after 1961. 17D is still in use and more than 400 million doses have been distributed. Little research has been done to develop new vaccines. Some researchers worry that the 60-year-old technology for vaccine production may be too slow to stop a major new yellow fever epidemic. Newer vaccines, based on vero cells, are in development and should replace 17D at some point.
Using vector control and strict vaccination programs, the urban cycle of yellow fever was nearly eradicated from South America. Since 1943 only a single urban outbreak in Santa Cruz de la Sierra, Bolivia, has occurred. But, since the 1980s, the number of yellow fever cases have been increasing again, and A. aegypti has returned to the urban centers of South America. This is partly due to limitations on available insecticides, as well as habitat dislocations caused by climate change. It is also because the vector control program was abandoned. Although no new urban cycle has yet been established, scientists believe that this could happen again at any point. An outbreak in Paraguay in 2008 was thought to be urban in nature, but this ultimately proved not to be the case.
In Africa, virus eradication programs have mostly relied upon vaccination. These programs have largely been unsuccessful because they were unable to break the sylvatic cycle involving wild primates. With few countries establishing regular vaccination programs, measures to fight yellow fever have been neglected, making the future spread of the virus more likely.
I love fireflies. When I see them on a warm evening flashing it takes me back to being a young girl running around my backyard with a jar and lid catching all the fireflies I could. I would then take the jar in the house to my bedroom and watch them flash. This is an article by Jason Bittle that I want to share with you. There’s more to a firefly that meets the eye. Enjoy
In the Great Smoky Mountains National Park in the eastern U.S., there’s a species of firefly (Photinus carolinis) that takes the showy spectacle to a new level.
In an attempt to woo a female, thousands of P. carolinis males flash their lanterns on and off at the same time, creating a synchronous bioluminescence display unlike any other on Earth. Every June, people come to the national park to witness the spectacle, which has become such a popular tourist attraction that you’d have an easier time getting into a Rolling Stones concert. Advance tickets sell out in a matter of minutes.
So for those of you who missed out on the natural light show this year, here are some amazing firefly facts to ponder on those warm summer nights. (See National Geographic’s photos of extreme summer adventures.)
Time Is of the Essence
For P. carolinis, the synchronous display is an event that’s simultaneously silent, rhythmic, tranquil, and frenetic, said Lynn Faust, a naturalist and the author of a forthcoming book called Fireflies, Glow-worms and Lightning Bugs: A Field Guide to the Fireflies of the Eastern U.S. and Canada.
“Peaceful to us,” she said, “life or death for them.”
Faust explains that synchronous fireflies live just two to four weeks after they reach their adult phase. That means each night is a desperate attempt to find a mate and pass on their genes. And if you’re a small black insect trying to find other small black insects in the dark, it helps to have a chemically activated beacon on your backend. (See other pictures of glowing animals.)
In P. carolinis, the synchrony goes like this: Around 9:30 p.m., a cloud of male fireflies starts to flash. Each male emits six quick blinks, then takes a break for about six seconds. Over time, the insects manage to coordinate their individual pulses to the point where the whole forest throbs neon green, then goes wordlessly dark.
The light show, as Faust calls it, is highly dependent on temperature, moisture level, and elevation—but given optimal conditions, the display can go on past midnight.
“Femme Fatale” Cannibals
Of course, there’s a downside to lighting up the night. As every little kid with a Mason jar knows, it makes the insects awfully easy to detect.
Among those taking notice are the females fireflies of another genus, Photuris. Entomologists have nicknamed these insects “femme fatales” because they eat P. carolinis fireflies—and they have some flashy ways of doing it.
Photuris fireflies attack synchronous fireflies in the air, a maneuver known as “hawking.” But that’s not how the femme fatales got their nickname.
“These fireflies flash the wrong signal and pretend like they’re a female Photinus carolinis,” said Rebecca Nichols, an entomologist for the Great Smoky Mountains National Park. “The male will come down thinking he’s going to mate, and then the Photuris will grab him and eat him.” (Related: “Flesh-Eaters: 5 Cannibalistic Animals.”)
The femme fatales are such skillful mimics that they can even switch between the flash signals of several species, depending on what’s fluttering around that night. Cannibalism offers extra nutrients to females at a time when they, too, will be mating and laying eggs, but a balanced diet isn’t the only thing they get out of the meal.
Many fireflies produce defensive compounds similar to the venom found in toads. Predators find these compounds distasteful and have learned to avoid eating fireflies altogether.
Fireflies in the genus Photuris don’t have these compounds, but research has shown they’re able to absorb them by eating other fireflies. What’s more, the chemical defenses also pass into the Photuris fireflies’ eggs to safeguard the next generation.
Synchronous fireflies aren’t totally defenseless though. When attacked by the femme fatales, the insects discharge a bit of their blood, which scientists call “reflex bleeding.”
For most predators, the blood offers a taste of the defensive compounds mentioned above and sends them packing, but for the femme fatale fireflies, it’s the stickiness that causes a problem. Faust wrote in 2012 in the Journal of Entomology that the blood “coagulates into a sticky mass” in the cannibal firefly’s mouth, sometimes giving the synchronous firefly enough time to escape.
But even reflex bleeding has a workaround. Faust has observed the femme fatales stalking and stealing fireflies from the webs of orb weaver spiders. These fireflies have already dispensed with their reflex bleeding and have been essentially gift-wrapped by the spider. The femme fatales will even do battle with the spider over a meal, though sometimes this means turning into a meal themselves.
Though the Smokies firefly display is pretty much over, luckily the species can be found throughout the southern Appalachian Mountains in the eastern U.S. In fact, Pennsylvania will be hosting its second-annual Firefly Festival later this month. And, of course, the bug is found around the world, especially in warm parts of Asia.
To Faust, seeing the synchronous fireflies “never gets old—it is a recurring miracle each year, just like the first wildflower, the fall leaves, the first hummingbird,” she said.
“I like to be up there the very first night the first male emerges and flashes. It gives me a kick and reassurance that life goes on.”